N-methyl-D-aspartate receptor (NMDAR) activity is involved in the processes of learning and memory. A novel antibody-based therapy developed by our lab targeting the NMDAR GluN1 subunit has previously been found to differentially modulate NMDAR function to improve learning and memory in 6-month-old and 22-month-old mice following passive transfer of IgG antibodies. We investigated genetic vaccination approaches using adeno-associated viral vectors (AAVs) as a mechanism of antigen delivery to produce therapeutic anti-GluN1 antibodies in vivo in mice and compared its effect to our existing polyclonal therapy. C57/BL6j mice received an intramuscular injection of AAV8 or AAV6 vectors expressing a recombinant GluN1 antigen (recGluN1) cDNA, with a luciferase transgene included as a control. Western blot analysis and ELISA assays were used to monitor the development of serum recGluN1 and luciferase antibodies at 8 weeks and 12 weeks post-vector injection. Learning and memory were assessed via the Morris Water Maze, Open Field Test, and Novel Object Recognition Test. Results from our pilot study demonstrated that AAV6 but not AAV8 vectors led to long-term antibody production following treatment. Serum antibodies reacted to recGluN1 epitopes similar to those produced in rats immunised with recGluN1 protein. Analysis of behavioural data is underway. However, current results suggest that this alternate approach to antibody production could facilitate long-term therapeutic studies and offer a method to rapidly screen similar immunotherapies in disease models.